Aging-Associated Dysfunction of AktProtein Kinase B S-Nitrosylation and Acetaminophen Intervention 英文参考文献.docVIP

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Aging-Associated Dysfunction of AktProtein Kinase B S-Nitrosylation and Acetaminophen Intervention 英文参考文献.doc

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Aging-Associated Dysfunction of AktProtein Kinase B S-Nitrosylation and Acetaminophen Intervention 英文参考文献

Aging-Associated Dysfunction ofAkt/Protein Kinase B: S-Nitrosylation and Acetaminophen Intervention MiaozongWu1,2,AnjaiahKatta3,MuraliK.Gadde1,2,HuaLiu1,2,5,SunilK.Kakarla3,JacquelineFannin3, SatyanarayanaPaturi1,2,RaviK.Arvapalli1,2,KevinM.Rice1,2,4,YelingWang1,2,6,EricR.Blough1,2,3,4 * 1DepartmentofBiologicalSciences,MarshallUniversity,Huntington,WestVirginia,UnitedStatesofAmerica,2CellDifferentiationandDevelopmentCenter,Marshall University, Huntington, West Virginia, United States of America, 3Department of Pharmacology, Physiology and Toxicology, Marshall University, Huntington, West Virginia, United States of America, 4Department of Exercise Science, Sport and Recreation, Marshall University, Huntington, West Virginia, United States of America, 5DepartmentofPhysiologyandPharmacology,SoutheastUniversity,Nanjing,China,6TheFirstHospital,JilinUniversity,Jilin,China Abstract Background:Agedskeletalmuscleischaracterizedbyanincreasedincidenceofmetabolicandfunctionaldisorders,whichif allowed to proceed unchecked can lead to increased morbidity and mortality. The mechanism(s) underlying the developmentofthesedisordersinagingskeletalmusclearenotwellunderstood.ProteinkinaseB(Akt/PKB)isanimportant regulatorofcellularmetabolismandsurvival,butitisunclearifagedmuscleexhibitsalterationsinAktfunction.Herewe report a novel dysfunction of Akt in aging muscle, which may relate to S-nitrosylation and can be prevented by acetaminophenintervention. PrincipalFindings:Comparedto6-and27-monthrats,thephosphorylationofAkt(Ser473andThr308)washigherinsoleus muscles of very aged rats (33-months). Paradoxically, these increases in Akt phosphorylation were associated with diminishedmammaliantargetofrapamycin(mTOR)phosphorylation,alongwithdecreasedlevelsofinsulinreceptorbeta (IR-b), phosphoinositide 3-kinase (PI3K), phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and phosphorylation of phosphoinositide-dependent kinase-1 (PDK1) (Ser241). In vitro Akt kinase measurements and ex